ArticleNucleic acids research2025
Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Polymerase face-off: emerging concepts in transcription-replication coordination.EMBO reports · 2026Review
- RAD51C-XRCC3 complex regulates FANCM-mediated R-loop resolution to safeguard genome integrity.Science advances · 2026Article
- A Quantitative DNA Fiber Assay to Monitor Replication Fork Progression, Protection, and Restart.Bio-protocol · 2026Article
- The Zinc Finger Ran-Binding Protein 3 (ZRANB3): An Advanced Perspective.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
RECQL5 helicase has been implicated in the regulation of homologous recombination (HR), replication stress responses, transcription elongation, and resolution of transcription-replication conflicts. However, the underlying mechanism by which RECQL5 regulates multiple functions in genome maintenance is obscure. Here, we find that RECQL5 localizes to the stalled fork sites and restricts RAD51-mediated excessive fork reversal to promote unrestrained DNA synthesis. The replication defect in the absence of RECQL5 can be rescued by co-depletion of SMARCAL1/ZRANB3/HLTF/FBH1 fork remodelers and expression of HR-defective mutants of RAD51. The RAD51 regulation at the stalled fork sites by RECQL5 requires its binding to PCNA, RAD51, and helicase activity and is independent of its interaction with RNAPII. Notably, the RECQL5 mutant devoid of its interaction with RAD51 regulates transcription elongation comparable to that of wild-type RECQL5. Collectively, our data demonstrates that RECQL5 distinctly regulates transcription elongation and RAD51-mediated fork remodelling to safeguard the replicating genomes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.